Structure - Function Flashcards
1
Q
What is the cup shaped around the glomerulus
A
BOWMAN’S CAPUSULE
2
Q
Smooth muscle cells found between / supporting glomerular capillaries, which can contract to regulate blood flow into the glomerulus.
They also have phagocytic properties similar to monocytes and release inflammatory cytokines and growth factors.
A
Mesangial Cells
3
Q
What is special about the glomerular capillaries
A
They are fenestrated, and allow large amounts of solute-rich fluid (Ions and large molecules, not protein or blood cells) to pass through
They have podocytes - which make up the visceral epithelium of bowman’s capsule
4
Q
Where does the filtrate enter the (bowman’s) capsular space
A
Filtration slits of the podocytes
5
Q
Clefts between the foot processes of the podocytes
A
Filtration slits
6
Q
Most nephrons are _____ They are the “hard workers” and have a shorter loop of henle
A
Cortical Nephrons
7
Q
About 15% of nephrons are ______ They have a long loop of henle
A
Juxtaglomerular Nephrons
8
Q
What do juxtaglomerular nephrons specialize in
A
CONCENTRATING URINE
9
Q
Where does renal filtration occur?
A
Glomerulus
10
Q
Where does renal reabsorption and secretion occur?
A
Tubules
11
Q
Name the two kinds of capillaries found in nephrons
A
Glomerular - filtration!
Peritubular -
12
Q
The only capillaries in the body that are fed and drained by an arteriole
A
Glomerular capillaries
13
Q
When filtrate reabsorbed by the tubules, how does it return to the blood stream
A
via peritubular capillaries
14
Q
What allows the blood pressure in the glomerular capillary bed to be so high?
A
The fact that these glomerular capillaries are fed and drained by an arteriole
15
Q
On what forces does glomerular filtration depend
A
STARLING forces - hydrostatic and osmotic pressures
16
Q
What makes glomeruli efficient filters?
A
- large surface area
- Surface is very permeable to water
- High glomerular BP (55 mmHg) (higher than capsule pressure)
17
Q
Glomerular BP?
A
55mmHg
18
Q
What opposes glomerular filtration?
A
Osmotic pressure in the plasma from protein
Fluid pressure in Bowman’s space
- Increase plasma protein (dehydration, polycythemia)
- Increase BS pressure
- Decrease BP
19
Q
What favors glomerular filtration?
A
Glomerular capillary BP
- raise systemic BP
- Decrease pressure in BS
- Decrease plasma protein (blood loss, no transfusion)
20
Q
Tubular cells are joined by _____ through which substances can _______
A
Tight junction, diffuse
21
Q
Percentage of urea reabsorbed
A
44%
22
Q
Percentage of Na reabsorbed
A
99.5%
23
Q
Percentage of water reabsorbed
A
99%
24
Q
Examples of things which are secreted in the tubules
A
H+
K+
Organic anions
25
Tubule secretion is particularly important for which homeostatic mechanism
Controlling blood pH (H+ secretion)
26
Normal GFR
90/120 ml/min
< 60 = disease
27
GFR affected by
1. Filtration surface area
2. Membrane permeability and Net Filtration Pressure (NFP)
3. Blood pressure / flow to glomerulus
28
Key mechanisms kidneys use to regulate water and ions
Water reabsorption
Na reabsorption / secretion
29
Range of daily urine volume
400 - 2500mL
30
Renal salt wasting
Hypo-aldosteronism
31
Order of operations in nephron
Afferent arteriole > glomerulus > Prox convoluted tubule > Descending loope of henle > Loop > thin ascending loop > thick ascending loop > distal convoluted tubule > (cortex, medulla) > Collecting duct > papilla of renal pyramid > minor and major calyces >renal pelvis (Hilum) > Ureter
32
What makes up the renal corpuscle
Glomerulus, bowman's capsule, mesangial cells
33
Major disorders that disrupt the glomerular filtration barrier
DMII, HTN, Glomerulonephritis (autoimmune)
34
Where does sodium reabsorption occur and how is it transported?
Occurs in all tubular segments EXCEPT the descending loop of Henle (for the countercurrent!)
Transported passively, by diffusion, from the tubular lumen to the epithelial cells. Then transported actively, via Na/K pump, from the epithelial cells to the systemic capillaries
35
By what mechanism is water reabsorbed
Osmosis (passive) - but ** determined by the movement of sodium and presence of aquaporins **
36
Sites for water / Na balance
Renal Tubules
37
Where would one find aquaporins?
Proximal convoluted tubule +++
Descending, loop, ascending?
NONE in collectinge ducts UNLESS YOU HAVE ADH
38
ADH is produced where and alongside what?
Produced in HYPOTHALAMUS
STORED in POSTERIOR PITUITARY
alongside oxytocin
39
How does ADH lead to increased aquaporins
increased plasma osmolarity > ADH from post pituitary >
binds receptors on basolateral membrane of COLLECTING DUCTS >
increased cAMP / PO4 >
AQP fuse w luminal membrane
40
How is sodium transported in renal tubules?
Transported passively, by diffusion, from the tubular lumen to the epithelial cells.
Then transported actively, via Na/K pump, from the epithelial cells to the systemic capillaries
41
Why is active transport of Na out of the tubule epithelial cells necessary?
To keep intracellular Na low and drive the diffusion gradient
42
Things which might disrupt the homeostasis of passive / active Na reabsorption and subsequent H20 / glucose drafting?
Broken AQPs
Lack of ATP in kidney
Tubular damage w interstitial fibrosis
43
How to baroreceptors in the atria and carotid arteries affect ADH
Lower BP at carotid / atrial baroreceptors will inhibit ADH, so the kidneys will hold on to water and increased blood volume / BP
44
How does SIADH affect fluid homeostasis
1. Too much ADH > too much water reabsorbed / retained
| 2. High BP, low Na
45
How does Diabetes Insipidus affect fluid homeostasis?
1. Not enough or ineffective ADH
2. Low BP, high Na
3. Large, dilute volumes urine
46
Where does concentration of urine happen/
Loop of Henle
47
What special function does the special structure of the loop of henle provide?
Countercurrent Multiplier
48
Osmolarity of filtrate in proximal tubule and beginning of descending loop vs plasma
IT'S THE SAME IT'S THE SAME
49
Describe how the osmolarity of filtrate changes throughout the tubules
PCT and beginning of descending loop (same as plasma)
Osmolarity increases (concentration) as filtrate travels down the descending limb - because only water is reabsorbed here. Impermeable to solutes.
Osmolarity decreases (dilutes) as filtrate travels up the ascending limb - because Na is reabsorbed. Permeable to solutes.
Filtrate entering the DCT is very dilute - as low as 70mOsm
Osmolarity either increases, decreases, or stays the same as filtrate travels down collecting duct - depending on body's needs, presence of ADH etc
50
What contributes to the medullary osmotic gradient
Urea recycling
51
How dilute can filtrate be by the time it reaches the DCT ?
Very dilute - as low as 70mOsm
52
How concentrated can urine become?
1200 mOsm
53
Key controller of Na reabsorption?
Aldosterone
54
Aldosterone site / action
Steroid, from adrenal cortex
Increases Na reabsorption from distal tubules and collecting ducts
** fine- tuning here - bulk reabsorption already happening in earlier tubules **
55
Increases Na reabsorption from distal tubules and collecting ducts by dumping K
Aldosterone
Hold Na, at the expense of K
56
JGA consists of
JG cells + Macula Densa
57
Enlarged, specialized smooth muscle cells that secrete renin and control blood flow to glomerulus
JG cells
58
Are JG cells considered endocrine?
YES
59
What kind of receptors to JG cells use to detect BP shifts in afferent arteriole?
Mechanoreceptors
60
How to renin and aldosterone relate?
JG cells detect Low BP > JG cells secrete Renin > Angiotensinogen / I / II > Aldosterone
61
A group of tall, closely packed cells in the DCT which detect changes in Na / osmolarity via chemoreceptors
Macula Densa
62
What does low Na in the DCT mean for Macula Densa?
Low Na = decreased filtration >> JG cells release renin (Paracrine signaling!!)
63
What controls aldosterone?
Renin, Angiotensin II >>
Adrenal Cortex >
Aldosterone >
Na and H20 retention
64
Three triggers for Renin release
1. Low BP (JGA, less stretch = more renin)
2. Low Na (Macula)
3. SNS stimulation (JG)
65
Atrial Natriuretic Peptide and Na
Increased BP > cardiac distention > ANP released
ANP > decreased aldosterone > Na dumped
ANP > afferent dilation, efferent constriction > Increased GFR
66
Major extracellular buffering system
CO2 / HCO3 system
67
Major intracellular buffers
Phosphate and proteins
68
How do the kidney's alter the body's pH?
By altering the plasma HCO3 concentration
HCO3 is filtered, then reabsorbed or secreted in tubules according to body's pH needs
Normally, all filtered HCO3 is "reabsorbed" (H exchange mechanism)
69
A "low oxygen" environment, this area of the kidney is particularly prone to ischemia
Medulla!
70
The structure of this area makes it particularly vulnerable to deposition of immune complexes, compliment fixation, and damage from HTN and glycosylation
Glomerulus!
| highly vascular, fenestrated structure
71
This area gets clogged by things that shouldn't have made it through the glomerulus and is therefore prone to ischemia
Tubules!
RBC, WBC, Protein, Fat, Stones
72
These structures are more prone to malformation, obstruction, and masses
"Post renal" structures - ureters, bladder
73
Renal medulla is particularly prone to what kind of problem
Ischemia
74
Glomerulus is particularly prone to what kinds of problems
Due to fenestrated vasculature:
Deposition of immune complexes, complement
HTN damage
Glycosylation
75
Tubules are particularly prone to
Ischemia, clogged by large molecules that make it through damaged glomeruli (WBC, RBC, protein etc)
76
Post renal structures are particularly prone to what kinds of problems
Malformation
Obstruction
Masses
77
What "pre renal" structures can cause renal problems?
Vascular - Renal Artery
General blood volume / perfusion
DRUGS (NSAIDs, ACEi, diuretics)
78
Heterogenous group of disorders characterized by rapid deterioration of renal function (GFR), rapid elevation of BUN, and S Cr, oliguria
ACUTE renal failure
79
Acute Renal Failure, Pre-renal causes (30%)
CV, volume depletion (ischemia)
Drug induced (NSAIDs, ACE, diuretics)
80
Acute Renal Failure, Intrarenal causes (60%)
Inflammatory diseases
Acute Tubular Necrosis
81
Acute Renal Failure, Post Renal causes (10%)
OBSTRUCTION
Cancer
Congenital abnormalities
82
60% of acute renal failure is caused by
Intrarenal problems, mostly Acute Tubular Necrosis
*ATN, when blood supply to kidney is severely reduced or blocked. Tubular cells slough off and form casts
83
30% of acute renal failure is caused by
Pre renal, hemodynamic
84
10% of acute renal failure is caused by
Post renal, OBSTRUCTION
85
Slow, progressive loss of renal function associated with:
Systemic diseases (HTN, DM, SLE) or
Intrinsic kidney disease (kidney stones, acute kidney injury, chronic glomerulonephritis, chronic pyelonephritis, obstructive uropathies, or vascular disorders)
Chronic Kidney Disease
86
Clinical definition of CKD
GFR less than 60 ml/min/1.73 m2 for 3 months or more
| Irrespective of the initial cause of the renal damage
87
Anatomical changes to kidney in CKD
Granular surface
Smaller size
Decreased function
high urine protein
88
Stage 1 CKD
GFR > 90
No obvious disease. GFR being compensated by higher kidney pressure
89
Stage 2 CKD
GFR 60-89
Early evidence of bone disease (VD3)
Creeping SrCr
EPO anemia
Mild HTN
90
Stage 3 CKD
GFR 30-59
Elevated SrCr and Urea
Mod HTN
High Triglycerides
Metabolic Acidosis
91
Stage 4 CKD
GFR 15-29
Hyperkalemia
Na / H2O retention
Increasing SrCr / Urea
92
Stage 5 CKD
GFR 0-14
Significant Uremia
Death
93
GFR for Kidney Failure
< 15
94
When do symptomatic changes appear in renal failure
Not until renal function declines to < 25% of normal (75% loss) - when adaptive reserves have bee exhausted
95
What causes the symptoms of renal failure
Symptoms result from:
increased levels of creatinine, urea, and potassium
alterations in salt and water balance
96
Intact nephron hypothesis
when nephrons are lost, the surviving nephrons step up their game to sustain normal kidney function
